The immune system and Cancer - Coggle Diagram
The immune system and Cancer
The Immune System
The first line of defense against invasion of pathogens
Required for the initiation of specific adaptive immune responses
Granulocytes such as NK cells and neutrophils
Macrophages or dendritic cells will ingest the pathogen and present the pathogenic antigens on either MHC class I or II.
These innate cells will travel to the lymph node via lymphatic vessels and activate CD8/CD4 T cells of the adaptive immune system
APC release cytokines upon interaction between APC and T cells to activate them.
A more specific immune response composed of specialized systemic cells to eliminate the infecting pathogen
Also creates immunological memory upon first response to enhance the immune response in future encounters
that will further differentiate through clonal expansion
Two types of pathways:
involves the secretion of antibodies by plasma cells and B lymphocytes that induces neutralization, opsonization and the activation of the complement system
APCs present the antigens to T helper cells to further activate more cytotoxic T cells that will induce apoptosis of the pathogen and infected cells.
The immune system recognizes cancer cells as foreign cells that should be eliminated.
Normal nucleated healthy cells that are infected will present the peptide antigens on the MHC class I.
The cell accumulates random mutations and becomes cancerous
There are two types of antigens that can be presented:
Tumour specific antigens:
Mutant peptides from mutated cellular proteins are presented
These types of antigens are only found on tumour cells
E.g Genetic mutation of Myc protein where the DNA sequence is altered that causes hyperactivity and promote cell cycle progression
Tumour associated antigens:
Antigens that are normally found in normal cells but are overexpressed in tumour cells or antigens presented are unique to tumour cells.
E.g Tyrosinase proteins that are produced in minute quantities in normal cells but are overexpressed in melanoma cells.
Killing of Cancer cells by Immune cells:
Antigen Presenting Cells and CD4 Helper T cells:
Tumour antigens are taken up by APCs where through phagocytosis of the tumour cells or released antigens and present them on MHC class II.
CD4 T helper cells will recognise the antigen and bind to the MHC class II of APC. Co-stimulatory molecules between these two will also interact (B7 on APC interact with CD28 of T cells) where it will release cytokines, IL2 to activate CD8 T cells that proliferate into cytotoxic T cells or activate itself.
CD4 T helper cells can also activate B cells through the release of IL10 and IL4
B cells get activated with the help of CD4 T helper cells and differentiate into plasma cells that secrete antibodies that can bind to antigens on the tumour.
Binding of antibodies on the tumour cells recruit natural killer cells to kill it by releasing perforin and granzymes
Antibodies are part of the humoral immunity pathway.
CD8 T cells:
Cytotoxic T cells activated by CD4 T helper cells contain receptors that can recognize tumor antigens presented on MHC class I of tumour cells
This will cause the release of perforins that will form pores on the tumour cells and secrete granzymes that enter these pores and degrade the cellular components of the tumour cell.
Engagement between Fas and FasL can also trigger apoptosis as they are death signals.
Involves the use of substances that are made from living organisms to help the immune system fight the cancer as the immune system has various mechanisms in fighting diseases.
Why is it needed?
The immune system can prevent and slow cancer growth, however, cancer cells are capable of escaping destruction by the immune system.
Cancer cells are able to avoid destruction caused by immune cells through a process known as Immunoediting and involves three phases,
where immune cells will cause their death but can also promote its growth.
Normal cells can become cancerous when they are exposed to carcinogens or acquire random mutations. E.g Reduced expression of p53 and Retinoblastoma proteins.
Upon acquiring and accumulating random mutations, they will be transformed cells and have various surface molecules such as
natural killer cell receptor ligands
comes in where the transformed cells are recognised by the immune cells due to the expressed surface molecules and get eliminated. E.g NKG2D on Natural killer cells will recognise the natural killer cell receptor ligands on the cancer cells and destroy it , suppressing the tumour cells
However, not all the tumour cells are eliminated. Those that are not eliminated will replicate with new mutations where they will not present the previous surface molecules to avoid detection by immune system. This is the
, this is where the cancer cells have escaped detection and are replicated and divided to increase tumour growth. The cancer cells may not be recognised by the tumour cells or become resistant to immune cell attacks as they acquire mutations that allow them to be undetected by the immune system or even inactivate the immune system
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Cancer is a disease caused by uncontrolled cell division due to the accumulation of mutations in cancer critical genes which can cause tumor growth and spread to surrounding tissues.